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Rumination and Affect Intensity Predict Glucocorticoid Reactivity to and Recovery from Acute Stress in Major Depression
Heightened emotional reactivity to stress is a cardinal feature of Major Depression. However, at the neurobiological level, depression is associated with both hyper-reactive and hypo-reactive (blunted) patterns of hypothalamic-pituitary-adrenal (HPA) axis response. Correctly interpreting these dissociated patterns requires an integration of neurohormonal parameters with cognitive-affective dynamics. Strong candidates for the latter include rumination, which involves prolongation of negative mood due to reduced ability to shift attentional focus from negative self-referential information, and high affect intensity, which involves strong changes in emotional reactivity. In our lab we use multi-level modeling techniques to examine trajectories of cortisol response to a social-evaluative laboratory stressor across time in samples ranging from early adolescence through adulthood. We find that depression is consistently associated with blunted cortisol reactivity relative to healthy comparisons. High brooding rumination was associated with significantly prolonged recovery of the cortisol response, and in adolescents this was specific to depression. Further, lower trait intensity of positive affective experience was associated with greater cortisol reactivity in the depressed group, but lower cortisol reactivity in the comparison group. An mechanistic discussion will be provided integrating additional moderators of HPA axis function that our lab has identified, including history of severe early life stress, glucocorticoid receptor polymorphisms, basal HPG hormones, and gender.